Effects of hemodilution on O2 transport in high-altitude polycythemia

Abstract

A native of the Peruvian Andes (4,250 m) was studied before and after isovolemic hemodilution of the hematocrit from 62 to 42%. O2 transport was studied with newly developed catheters in the radial and pulmonary arteries. These catheters allowed continuous measurement of arteriovenous O2 content and intermittent cardiac output by thermodilution. During exercise tests, breath-by-breath gas exchange measurements also allowed cardiac output to be calculated by the O2-Fick technique. A complex series of interrelated physiological changes occurred in response to hemodilution. These included increased ventilation, increased arterial and mixed venous PO2, increased cardiac output (both heart rate and stroke volume), and improved ventilation-flow match. The general improvement in symptoms that followed hemodilution correlated well with increased anaerobic threshold and mixed venous PO2 during exercise.

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

“…This is because the associated increase in blood viscosity produces a higher peripheral vascular resistance that might compromise Q, thereby reducing V O2,max (Guyton and Richardson, 1961;Connes et al, 2006). It is reasonable to expect that a moderately increased Hct could confer a physiological advantage under hypoxia because a greater quantity of O 2 can be carried at partial saturations, but experimental results do not support this (McGrath and Weil, 1978;Winslow et al, 1985). In humans at high altitude, evidence suggests that the optimal Hb concentration might actually be quite close to the typical sea level value (Villafuerte et al, 2004).…”

“…For example, in Andean natives living at altitudes of >3000m, Hct and Hb concentrations can reach values of up to 0.83 and 270gl -1 , respectively (Bouverot, 1985). This excessive polycythemia limits exercise performance, Q and pulmonary function, and appears to play a key role in the pathogenesis of chronic mountain sickness (Winslow et al, 1985;Monge and León-Velarde, 1991;Rivera-Ch et al, 2007). Richards (Richards, 1960) provided a vivid description of the effects of hypoxia-induced polycythemia in patients suffering from chronic pulmonary disease: "The increased red cell mass produces increased blood volume, which overfills the heart; and this organ, already under strain working against a restricted pulmonary vascular bed, goes into congestive heart failure, which still further increases blood volume.…”

Anemia in Critical Illness

“…Even more severe anemia may be tolerable with chronicity due to changes at the cellular level driven by transcription of genes enhancing hypoxic survival, such as those regulated by hypoxia-inducible factor (HIF) (32). In patients with chronic obstructive pulmonary disease (COPD), there is higher minute ventilation with anemia (33), and conversely, less ventilation with polycythemia in healthy persons during exercise (34). The extent to which these impressive compensatory changes can occur in critically ill and injured patients is unknown.…”

The Heart and Pulmonary Circulation at High Altitudes

“…28,54 Bloodletting alone or isovolemic hemodilution are palliative procedures to reduce the exaggerated polycythemia with partial improvement of signs and symptoms. 88,89 Other procedures are directed to improve ventilation with respiratory stimulant drugs such as medroxyprogesterone and acetazolamide, with consequent reduction of hematocrit and improvement of symptomatology. 66,90 Vasodilators are being tested to reduce high-altitude PH.…”